Evolution of the human lifespan and diseases of aging: Roles of infection, inflammation, and nutrition

被引:233
作者
Finch, Caleb E. [1 ,2 ]
机构
[1] Davis Sch Gerontol, Los Angeles, CA 90089 USA
[2] Univ So Calif, Los Angeles, CA 90089 USA
关键词
chimpanzee; pathology; CHIMPANZEE PAN-TROGLODYTES; APOLIPOPROTEIN-E; POSITIVE SELECTION; ALZHEIMER-DISEASE; WILD CHIMPANZEES; CARDIOVASCULAR-DISEASE; SPONTANEOUS NEOPLASIA; REPRODUCTIVE-TRACT; NONHUMAN-PRIMATES; OXIDATIVE STRESS;
D O I
10.1073/pnas.0909606106
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Humans have evolved much longer lifespans than the great apes, which rarely exceed 50 years. Since 1800, lifespans have doubled again, largely due to improvements in environment, food, and medicine that minimized mortality at earlier ages. Infections cause most mortality in wild chimpanzees and in traditional forager-farmers with limited access to modern medicine. Although we know little of the diseases of aging under premodern conditions, in captivity, chimpanzees present a lower incidence of cancer, ischemic heart disease, and neurodegeneration than current human populations. These major differences in pathology of aging are discussed in terms of genes that mediate infection, inflammation, and nutrition. Apolipoprotein E alleles are proposed as a prototype of pleiotropic genes, which influence immune responses, arterial and Alzheimer's disease, and brain development.
引用
收藏
页码:1718 / 1724
页数:7
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